An arylthiazyne derivative is a potent inhibitor of lipid peroxidation and ferroptosis providing neuroprotection in vitro and in vivo

Sci Rep. 2021 Feb 10;11(1):3518. doi: 10.1038/s41598-021-81741-3.

Abstract

Lipid peroxidation-initiated ferroptosis is an iron-dependent mechanism of programmed cell death taking place in neurological diseases. Here we show that a condensed benzo[b]thiazine derivative small molecule with an arylthiazine backbone (ADA-409-052) inhibits tert-Butyl hydroperoxide (TBHP)-induced lipid peroxidation (LP) and protects against ferroptotic cell death triggered by glutathione (GSH) depletion or glutathione peroxidase 4 (GPx4) inhibition in neuronal cell lines. In addition, ADA-409-052 suppresses pro-inflammatory activation of BV2 microglia and protects N2a neuronal cells from cell death induced by pro-inflammatory RAW 264.7 macrophages. Moreover, ADA-409-052 efficiently reduces infarct volume, edema and expression of pro-inflammatory genes in a mouse model of thromboembolic stroke. Targeting ferroptosis may be a promising therapeutic strategy in neurological diseases involving severe neuronal death and neuroinflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Cell Death / drug effects*
  • Cell Death / physiology
  • Ferroptosis / drug effects*
  • Ferroptosis / physiology
  • Glutathione / metabolism
  • Iron / metabolism
  • Lipid Peroxidation / drug effects*
  • Microglia / drug effects
  • Microglia / metabolism
  • Neuroprotection / drug effects
  • Phospholipid Hydroperoxide Glutathione Peroxidase / metabolism
  • Phospholipid Hydroperoxide Glutathione Peroxidase / pharmacology
  • Protective Agents / pharmacology*

Substances

  • Protective Agents
  • Iron
  • Phospholipid Hydroperoxide Glutathione Peroxidase
  • Glutathione